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Glioblastoma

A plain-English summary of the published research on Glioblastoma, reviewed and approved by our editors — not a hand-curated clinical overview.

Research summary · reviewed
Educational only: This page is not medical advice. Coordinate decisions with your oncology team.

Reviewed Jun 2026 · OncoForge editorial · How we review →

AI extractedhuman reviewedsources checkedretractions suppressed· last updated Jun 2026

Evidence at a glanceHuman trial / meta-analysisMixed results⚠ Studies disagree
54 published studies that name Glioblastoma7 human studies approved & graded (trial, observational, or meta-analysis)161 human clinical studies in the Glioblastoma corpus1395 source documents in the Glioblastoma corpus

last checked June 19, 2026

Why this grade?

Human trial / meta-analysis — Includes human trial or meta-analysis evidence.

Computed deterministically from the studies’ types and reported outcomes — not written by AI, and not a claim that anything works.

What the guidelines say

NCI PDQESMONCCNASCO

We link the authoritative guidelines rather than reproduce them. Below, the treatments on this page are split into standard care, guideline or regulatory options, supportive care, and studied but not standard so established care is not mixed with experimental or supportive items.

Guideline / FDA options - context-specific
  • Temozolomide
  • Bevacizumab
Studied, not standard - investigational
  • Doxorubicin
  • Eribulin
  • lomustine (CCNU)
  • dendritic cell vaccine
  • IL-12-armed oncolytic herpes simplex virus (oHSV:IL-12)
  • oncolytic herpes simplex virus (oHSV)
  • ?
  • Best supportive care
  • CRISPRi TERT silencing
  • Graphene quantum dots (GQDs)
  • supervised aerobic and resistance exercise
  • 5-aminolevulinic acid (5-ALA) fluorescence-guided surgery
  • gross total resection (GTR)
  • intraoperative radiotherapy
  • Maximal safe surgical resection
  • Supratotal resection (SpTR)
  • Surgical resection (extent of resection)
  • Tumor Treating Fields (alternating electric field therapy)
  • tumor treating fields (TTF)
  • Hypofractionated radiotherapy plus temozolomide
  • Radiotherapy
  • Suramin
  • Butylidenephthalide (BP)
  • Costunolide
  • Epigallocatechin gallate (EGCG)
  • Resveratrol
  • Thymoquinone
  • Arsenico
  • axitinib
  • BIBR1532
  • curcumin
  • plumbagin
  • genistein
  • trichostatin A (TSA)
  • MST-312
  • MZ-5-156 (GH-RH antagonist)
  • Pembrolizumab

Read the guidelines

Cancer-specific deep links aren’t curated yet — these search the authoritative sources for Glioblastoma.

Treatment map: Glioblastoma

Open as a full page →

Standard care plus every compound studied in the literature (each cited) and graded by evidence, organized by clinical readiness. A category, not a verdict that anything works — confirm anything here with your oncology team.

45
Interventions
0
Standard of care
37
Tested in people
0
Lab / animal
1
Named in lit.
8
Classes
Standard of care (0) Guideline option (7) Tested in people (37) Lab / animal only (0) Named in the literature (1)

Tested in people, by trial phase: Phase II ×1 · phase not reported ×36

Clinical evidence
Preclinical evidence
Standard of care
Guideline option
Tested in people
Lab / animal only
Named in the literature
Surgery & procedures
—
—
7
—
1
Radiotherapy
—
—
3
—
—
Chemotherapy
—
5
3
—
—
Targeted therapy
—
1
9
—
—
Immunotherapy
—
—
4
—
—
Repurposed drugs
—
—
1
—
—
Supplements & natural agents
—
—
5
—
—
Other
—
1
5
—
—

Columns group into clinical evidence (used in, or tested on, people) and preclinical evidence (lab/animal, or only named in the literature). Cell = number of interventions; a dashed cell means none recorded there.

Established care — detail (7)
Chemotherapy
TemozolomideAdjuvant (after surgery) · IDH-wildtype
FDA-approved for this cancer.
—Guideline option
temozolomideAdjuvant (after surgery)
FDA-approved for this cancer.
—Guideline option
TemozolomideMaintenance
FDA-approved for this cancer.
—Guideline option
temozolomideFirst-line (advanced disease)
FDA-approved for this cancer.
—Guideline option
TemozolomideAdjuvant (after surgery) · methylation at the O6-methylguanine-DNA methyltransferase (MGMT) promoter in cancer DNA
FDA-approved for this cancer.
—Guideline option
Targeted therapy
Bevacizumab
FDA-approved for this cancer.
—Guideline option
Other
Temozolomide
FDA-approved for this cancer.
—Guideline option
Investigational & adjunct compounds — detail (38)
Phase II trial (1)
Pembrolizumaboff-label
Meta-analysis (36)
?5-aminolevulinic acid (5-ALA) fluorescence-guided surgeryArsenicoaxitinibBest supportive careBIBR1532Butylidenephthalide (BP)CostunolideCRISPRi TERT silencingcurcumindendritic cell vaccineDoxorubicinoff-labelEpigallocatechin gallate (EGCG)Eribulin· TERT mutationsgenisteinGraphene quantum dots (GQDs)· Neoadjuvant (before surgery)gross total resection (GTR)Hypofractionated radiotherapy plus temozolomideIL-12-armed oncolytic herpes simplex virus (oHSV:IL-12)intraoperative radiotherapylomustine (CCNU)Maximal safe surgical resection· Adjuvant (after surgery)MST-312MZ-5-156 (GH-RH antagonist)oncolytic herpes simplex virus (oHSV)plumbaginRadiotherapy· Adjuvant (after surgery)RadiotherapyResveratroloff-labelsupervised aerobic and resistance exercise· Adjuvant (after surgery)Supratotal resection (SpTR)SuraminThymoquinonetrichostatin A (TSA)Tumor Treating Fields (alternating electric field therapy)· First-line (advanced disease)tumor treating fields (TTF)
Named in the literature
Surgical resection (extent of resection)· First-line (advanced disease)

"Tested in people" rows show the highest trial phase found in that compound's cited human studies (Phase I–IV; "phase not reported" = a human study with no phase tag). "Studied" = named in the cited literature for this cancer. "FDA ✓" = FDA-approved for this cancer; "off-label" = an FDA-approved drug used outside its approved indications (per openFDA). Not a claim that anything works.

Reported figures

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Snapshot

The essentials in ~60 seconds — every line is drawn from the cited sources below.

What it is
Glioblastoma is a World Health Organization grade IV glioma — a common, highly aggressive primary brain tumor described as among the most lethal brain tumours. [1][2][3][4]
Survival
Median overall survival is reported as about 12–18 months; long‑term survival is poor, with five‑year survival reported as low (below 10% in some summaries and less than 5% in others). [1][4][5]
Standard treatment
Initial management commonly is maximal safe surgical resection or biopsy followed by radiotherapy with concurrent and adjuvant temozolomide (the Stupp protocol); surgery, radiation and chemotherapy are central, with adjuncts such as 5‑ALA fluorescence guidance and tumour treating fields mentioned in contemporary care. [6][2][7][5][8][9]
Key test
Molecular biomarker testing including IDH status and markers such as TERT promoter mutation, EGFR amplification, and chromosome 7 gain/10 loss is used to define molecular glioblastoma and is essential for diagnosis and classification. [10][11]
Biggest challenge
Frequent early recurrence, treatment resistance and marked inter‑ and intra‑tumour heterogeneity lead to very poor long‑term survival and an urgent need for new effective therapies. [6][9][8][4]

Ask about Glioblastoma

Answers come only from the cited sources on this page — with the supporting evidence shown. If the sources here don't cover your question, it will say so. Educational information, not medical advice.

Key numbers & factors

Risk factors

  • ▲ increases riskIncreasing age — Pooled analysis: HR = 1.03 [1.00, 1.05] for decreased survival [1]
  • ▼ lowers riskElevated circulating FGF21 — Mendelian randomization associated with reduced risk of glioblastoma [9]
  • ▲ increases riskIncreased circulating TNF‑β — Mendelian randomization reported a possible link to increased risk [9]
  • ▲ increases riskHigh preoperative platelet-to-lymphocyte ratio (PLR) — Pooled HR = 1.46, 95% CI [1.23, 1.74] for worse overall survival [12]
  • ▲ increases riskHigher preoperative platelet count — Borderline predictor of worse overall survival (pooled HR = 1.38, 95% CI [1.00, 1.90]) [12]
  • ◆ mixedSocioeconomic factors (SES, race, insurance, area of residence) — Associated with differences in incidence and survival and may confound outcomes [13]

Biomarkers

  • MGMT promoter methylation / MGMT expressionActionablePredicts sensitivity to temozolomide and informs treatment selection (e.g., radiotherapy alone vs temozolomide in certain older patients) [5][8][14]
  • TERT (hTERT) promoter mutationActionableMost prevalent oncogenic mutation in GBM and one of the molecular markers used to define molecular glioblastoma in IDH‑wildtype lower‑grade gliomas [8][10]
  • EGFR amplificationActionableMarker used to define molecular glioblastoma in IDH‑wildtype lower‑grade gliomas [10]
  • Chromosome 7 gain / chromosome 10 lossActionableCombined copy‑number aberrations used to define molecular glioblastoma in IDH‑wildtype lower‑grade gliomas [10]
  • p53 status (imaging-predicted) · Radiomics models can predict p53 status from MRI (modest pooled performance) [15]
  • MicroRNAs (e.g., miR‑221, miR‑222, miR‑132, miR‑125b, miR‑21, miR‑10b) · Associated with chemoresistance and with bevacizumab response in research studies [16]
  • Preoperative blood markers (PLR, platelet count) · Associated with overall survival in pooled analyses [12]

10 sections — tap any heading to expand its cited detail. Key points are above.

Overview6 points
  • Sources describe GBM as a World Health Organization grade IV glioma and a prevalent, notably aggressive brain tumor; it is reported as among the most lethal brain tumors. [1][2][3][4]4 sources
  • Median overall survival is reported as about 12–18 months, and five-year survival is below 10%. [1][4]
  • The current standard of care commonly is maximal safe surgical resection or biopsy followed by radiotherapy with concurrent and adjuvant temozolomide chemotherapy (the 'Stupp protocol'); overall, standard therapy commonly combines surgery, radiation therapy, and chemotherapy. [6][2]
  • The EANO guideline provides recommendations for diagnostic and therapeutic procedures for patients with malignant gliomas. [17]
  • The WHO 2021 classification defines IDH wild type histologically lower-grade glioma as molecular glioblastoma when specified molecular alterations are present. [10]
  • Supratotal resection (SpTR) is described as an emerging surgical concept aiming to achieve a more extensive resection than conventional techniques. [18]
Key biomarkers8 points
  • MGMT-related markers influence response to temozolomide and treatment selection: overexpression of the DNA repair gene MGMT is reported to reduce glioblastoma sensitivity to temozolomide; MGMT promoter methylation was associated with an augmentation in median survival from 12.1 to 14.6 months after adding temozolomide to postoperative radiotherapy; and ASCO-SNO states that for older patients with poor performance status or concerns about toxicity or prognosis, radiotherapy alone is reasonable for MGMT promoter–unmethylated tumors while temozolomide alone is reasonable for MGMT promoter–methylated tumors. [5][8][14]3 sources
  • Molecular biomarkers are considered essential and are evolving to facilitate diagnosis and therapeutic decision-making in glioblastoma. [11]
  • Mutations in the telomerase reverse transcriptase (hTERT) promoter are the most prevalent oncogenic mutation in glioblastoma, affecting up to 80% of cases; unlike other genetic changes, hTERT promoter mutations were observed to be clonal events in most cases and remained consistent between samples taken before and after treatment. [8]
  • Magnetic-resonance-imaging-based radiomics models showed modest pooled diagnostic performance for predicting glioma p53 status, with exclusive radiomics models achieving a pooled AUROC of 0.72 and combined models (radiomics plus complementary features) achieving a pooled AUROC of 0.89. [15]
  • Preoperative blood-derived markers were associated with overall survival in pooled analyses: high preoperative platelet-to-lymphocyte ratio (PLR) was associated with worse overall survival (pooled HR = 1.46, 95% CI [1.23, 1.74]), and higher preoperative platelet count was a borderline predictor of worse overall survival (pooled HR = 1.38, 95% CI [1.00, 1.90]). [12]
  • Significantly upregulated microRNAs validated in chemoresistant glioblastoma included miR-221, miR-222, miR-132, and miR-125b; miR-21 and miR-10b were reported as the most replicated microRNAs for assessing bevacizumab response, with low expression in Avastin-resistant GBM. [16]
  • Mendelian randomization analyses reported that elevated circulating fibroblast growth factor 21 (FGF21) was associated with a reduced risk of glioblastoma, while increased circulating tumor necrosis factor β (TNF-β) was reported as possibly linked to an increased risk of glioblastoma. [9]
  • TERT promoter mutation, EGFR amplification, or chromosome seven gain and ten loss aberrations are listed as molecular markers that define molecular glioblastoma in IDH wild-type lower-grade gliomas. [10]
Standard management6 points

Key figures

Survival & outcomes
OutcomeValue95% CI
median overall survival with addition of temozolomide14.6 months—
PTV margin3—
CTV margin20—
CTV margin15—
Source quotes
  • “This augmentation in median survival from 12.1 to 14.6 months was particularly beneficial to patients with methylation at the O6-methylguanine-DNA methyltransferase (MGMT) promoter in cancer DNA [3].”
  • “A PTV margin based on the individual mask system and IGRT procedures available is advised; this should usually be no greater than 3mm when using IGRT.”
  • “Based on the EORTC recommendation focusing on the resection cavity and residual enhancing regions on T1-sequences with the addition of a 20mm margin, special situations are presented with corresponding potential adaptations depending on the specific clinical situation.”
  • “Based on the EORTC recommendation focusing on the resection cavity and residual enhancing regions on T1-sequences with the addition of a reduced 15mm margin, special situations are presented with corresponding potential adaptations depending on the specific clinical situation.”
  • The current standard of care at initial diagnosis is maximal safe surgical resection or biopsy followed by radiotherapy with concurrent and adjuvant temozolomide (the Stupp protocol); since 2005 this commonly consists of concomitant radiotherapy and temozolomide for 6 weeks followed by maintenance chemotherapy for 6 months. [6][3][7][5][8]5 sources
  • Consensus recommendations define the clinical target volume based on postoperative contrast-enhanced T1 abnormalities, focusing on the resection cavity and residual enhancing regions on T1 sequences with isotropic margins and without the need to cone down; ESTRO-ACROP (2016) describes the addition of a 20mm margin and ESTRO-EANO (2023) describes the addition of a reduced 15 mm margin. ESTRO-EANO advises that a planning target volume (PTV) margin based on the individual mask system and IGRT procedures should usually be no greater than 3 mm when using IGRT. [19][20]
  • Sources state that extent of resection (EOR) is routinely determined by postoperative MRI; EOR may be associated with survival and can affect epilepsy, neurocognition, quality of life, neurological status, and planning of radiation and pharmacotherapy, with level A recommendations for resection of newly diagnosed glioblastomas. [21][3]
  • Contemporary management summaries include the use of 5-aminolevulinic acid (5-ALA) fluorescence guidance to optimize resection and tumor treating fields (TTFields) as adjuncts in modern care; TTFields are mentioned alongside surgery, radiotherapy, and chemotherapy among interventions used for GBM. [6][9]
  • The addition of temozolomide to postoperative radiotherapy augmented median survival from 12.1 to 14.6 months. [8]
  • Conventional magnetic resonance imaging is the standard imaging modality for diagnosis and surgical planning but has shortcomings that can obscure early identification of infiltrating tumor. [3]
Treatments & compounds studied43 treatments

Chemotherapy

  • lomustine (CCNU): Lomustine (CCNU) has been used as a comparator or control treatment in randomized trials of progressive GBM. [7]
  • Temozolomide · 5 findings
    • Adjuvant (after surgery) · IDH-wildtypeTemozolomide (TMZ) is recommended concurrently with radiotherapy for patients with newly diagnosed glioblastoma, IDH-wildtype, CNS WHO grade 4 followed by 6 months of adjuvant TMZ. [14]
      adjuvant duration 6 monthsstandard RT duration comparator 6 vs 6-week RT plus TMZ
      Source quotes
      • “Concurrent TMZ and RT should be offered to patients with newly diagnosed glioblastoma, IDH-wildtype, CNS WHO grade 4 followed by 6 months of adjuvant TMZ.”
      • “In situations in which the benefits of 6-week RT plus TMZ may not outweigh the harms, hypofractionated RT plus TMZ is reasonable.”
    • Adjuvant (after surgery) · methylation at the O6-methylguanine-DNA methyltransferase (MGMT) promoter in cancer DNAAddition of temozolomide (TMZ) to postoperative radiotherapy was associated with an increase in median survival from 12.1 to 14.6 months, an effect reported to be particularly pronounced in patients with methylation at the O6-methylguanine-DNA methyltransferase (MGMT) promoter. [8]
      median overall survival with addition of temozolomide 14.6 vs 12.1 months vs postoperative radiotherapy alone
      Source quote
      • “This augmentation in median survival from 12.1 to 14.6 months was particularly beneficial to patients with methylation at the O6-methylguanine-DNA methyltransferase (MGMT) promoter in cancer DNA [3].”
    • Adjuvant (after surgery)Concurrent and adjuvant temozolomide (TMZ) is described as part of the Stupp protocol alongside radiotherapy. [6]
    • MaintenanceTemozolomide chemotherapy is administered concomitantly with radiotherapy for 6 weeks followed by maintenance chemotherapy for 6 months in the Stupp protocol. [3]
    • First-line (advanced disease)Sources report that temozolomide (TMZ) appears in randomized trials for progressive glioblastoma, including as part of combinations such as Depatux‑M + TMZ. [7]
Show 2 lab & early-research entries
  • Doxorubicin: Doxorubicin has been used in preclinical glioblastoma models combined with graphene quantum dots (GQDs) or photothermal therapy and was reported to cause increased cell mortality after GQD pretreatment. [22]
  • Eribulin: TERT mutationsTakahashi et al. tested the effectiveness of Eribulin mesylate against GBM cells with TERT mutations in preclinical studies. [8]
    median overall survival with addition of temozolomide 14.6 vs 12.1 months vs postoperative radiotherapy alone
    Source quote
    • “This augmentation in median survival from 12.1 to 14.6 months was particularly beneficial to patients with methylation at the O6-methylguanine-DNA methyltransferase (MGMT) promoter in cancer DNA [3].”

Targeted therapy

  • Arsenico: Cheng et al. reported investigation of arsenic (Arsenico) as an indirect hTERT inhibitor in glioma studies. [8]
    telomerase activity reduction 50%recovery of basal telomerase activity after withdrawal 95%
    Source quotes
    • “When medulloblastoma cells (ONS76) and GBM multiforme cell lines (M059K, KNS60) were treated with MST-312, the telomerase activity was reduced by approximately 50% (the TRAP assay).”
    • “Interestingly, when MST-312 was withdrawn, there was a 95% recovery of basal telomerase activity within 72 h, indicating that MST-312 acts as a competitive telomerase inhibitor in brain tumor cells.”
  • Bevacizumab: ASCO–SNO guidance states bevacizumab is not recommended; miR-21 and miR-10b have been examined for bevacizumab response; some progressive GB trials included bevacizumab-containing arms. [14][16][7]3 sources
    adjuvant duration 6 monthsstandard RT duration comparator 6 vs 6-week RT plus TMZHR for death (targeted therapy vs bevacizumab) 1.08 (95% CI 0.92–1.26), p = 0.3759 vs bevacizumab
    Source quotes
    • “Concurrent TMZ and RT should be offered to patients with newly diagnosed glioblastoma, IDH-wildtype, CNS WHO grade 4 followed by 6 months of adjuvant TMZ.”
    • “In situations in which the benefits of 6-week RT plus TMZ may not outweigh the harms, hypofractionated RT plus TMZ is reasonable.”
    • “A mortality risk of 1.08 (95% CI 0.92–1.26, p = 0.3759) demonstrated that there was no significant difference of mortality for patients who were treated with a targeted therapy compared to bevacizumab alone (n = 1268, Figure 2C).”
Show 8 lab & early-research entries
  • axitinib: Preclinical combinations of IL-12-armed oHSV with the VEGFR inhibitor axitinib showed greater antitumor effects than either monotherapy in human and murine glioblastoma stem-like cell models. [23]
  • BIBR1532: BIBR1532, a non-peptidic, non-nucleoside small molecule telomerase inhibitor, demonstrated a dose-dependent reduction in cell viability and induced cytotoxicity when administered across a wide dose range (25–200 μM). [8]
    telomerase activity reduction 50%recovery of basal telomerase activity after withdrawal 95%
    Source quotes
    • “When medulloblastoma cells (ONS76) and GBM multiforme cell lines (M059K, KNS60) were treated with MST-312, the telomerase activity was reduced by approximately 50% (the TRAP assay).”
    • “Interestingly, when MST-312 was withdrawn, there was a 95% recovery of basal telomerase activity within 72 h, indicating that MST-312 acts as a competitive telomerase inhibitor in brain tumor cells.”
  • curcumin: Khaw et al. tested curcumin on GBM cell lines and reported that it reduced hTERT mRNA levels via transcription inhibition. [8]
    telomerase activity reduction 50%recovery of basal telomerase activity after withdrawal 95%
    Source quotes
    • “When medulloblastoma cells (ONS76) and GBM multiforme cell lines (M059K, KNS60) were treated with MST-312, the telomerase activity was reduced by approximately 50% (the TRAP assay).”
    • “Interestingly, when MST-312 was withdrawn, there was a 95% recovery of basal telomerase activity within 72 h, indicating that MST-312 acts as a competitive telomerase inhibitor in brain tumor cells.”
  • plumbagin: Khaw et al. tested plumbagin on GBM cell lines and reported that it reduced hTERT mRNA levels via transcription inhibition. [8]
    telomerase activity reduction 50%recovery of basal telomerase activity after withdrawal 95%
    Source quotes
    • “When medulloblastoma cells (ONS76) and GBM multiforme cell lines (M059K, KNS60) were treated with MST-312, the telomerase activity was reduced by approximately 50% (the TRAP assay).”
    • “Interestingly, when MST-312 was withdrawn, there was a 95% recovery of basal telomerase activity within 72 h, indicating that MST-312 acts as a competitive telomerase inhibitor in brain tumor cells.”
  • genistein: Khaw et al. tested genistein on GBM cell lines and reported that it reduced hTERT mRNA levels via transcription inhibition. [8]
    telomerase activity reduction 50%recovery of basal telomerase activity after withdrawal 95%
    Source quotes
    • “When medulloblastoma cells (ONS76) and GBM multiforme cell lines (M059K, KNS60) were treated with MST-312, the telomerase activity was reduced by approximately 50% (the TRAP assay).”
    • “Interestingly, when MST-312 was withdrawn, there was a 95% recovery of basal telomerase activity within 72 h, indicating that MST-312 acts as a competitive telomerase inhibitor in brain tumor cells.”
  • trichostatin A (TSA): Khaw et al. tested trichostatin A (TSA) on GBM cell lines and reported that it reduced hTERT mRNA levels via transcription inhibition. [8]
    telomerase activity reduction 50%recovery of basal telomerase activity after withdrawal 95%
    Source quotes
    • “When medulloblastoma cells (ONS76) and GBM multiforme cell lines (M059K, KNS60) were treated with MST-312, the telomerase activity was reduced by approximately 50% (the TRAP assay).”
    • “Interestingly, when MST-312 was withdrawn, there was a 95% recovery of basal telomerase activity within 72 h, indicating that MST-312 acts as a competitive telomerase inhibitor in brain tumor cells.”
  • MST-312: MST-312, a chemically modified derivative of EGCG, reduced telomerase activity by approximately 50% in medulloblastoma and GBM cell lines but produced a 95% recovery of basal telomerase activity within 72 h after withdrawal. [8]
    telomerase activity reduction 50%recovery of basal telomerase activity after withdrawal 95%
    Source quotes
    • “When medulloblastoma cells (ONS76) and GBM multiforme cell lines (M059K, KNS60) were treated with MST-312, the telomerase activity was reduced by approximately 50% (the TRAP assay).”
    • “Interestingly, when MST-312 was withdrawn, there was a 95% recovery of basal telomerase activity within 72 h, indicating that MST-312 acts as a competitive telomerase inhibitor in brain tumor cells.”
  • MZ-5-156 (GH-RH antagonist): The growth hormone‑releasing hormone (GH‑RH) antagonist MZ‑5‑156 significantly reduced hTERT expression and telomerase activity in glioma U87MG cells both in vitro and in vivo. [8]
    telomerase activity reduction 50%recovery of basal telomerase activity after withdrawal 95%
    Source quotes
    • “When medulloblastoma cells (ONS76) and GBM multiforme cell lines (M059K, KNS60) were treated with MST-312, the telomerase activity was reduced by approximately 50% (the TRAP assay).”
    • “Interestingly, when MST-312 was withdrawn, there was a 95% recovery of basal telomerase activity within 72 h, indicating that MST-312 acts as a competitive telomerase inhibitor in brain tumor cells.”

Immunotherapy

  • dendritic cell vaccine: Dendritic cell vaccine combined with standard care was associated with improved overall survival (HR = 0.71; 95% CI, 0.57–0.88) and improved progression-free survival (HR = 0.65; 95% CI, 0.43–0.98) in pooled trials. [24]
    HR for overall survival (DC vaccine + standard care vs standard care) 0.71 (95% CI 0.57–0.88) vs standard careHR for progression-free survival (DC vaccine + standard care vs standard care) 0.65 (95% CI 0.43–0.98) vs standard care
    Source quotes
    • “DC vaccine plus standard care was associated with significantly improved OS (HR = 0.71; 95% CI, 0.57 - 0.88)”
    • “DC vaccine plus standard care was associated with significantly improved OS (HR = 0.71; 95% CI, 0.57 - 0.88) and PFS (HR = 0.65; 95% CI, 0.43 - 0.98).”
Show 2 lab & early-research entries
  • IL-12-armed oncolytic herpes simplex virus (oHSV:IL-12): In preclinical immunocompetent syngeneic mouse glioblastoma models, IL-12-armed oncolytic herpes simplex virus (oHSV:IL-12) converted otherwise inactive viral therapy into a durable immunotherapy with sustained macrophage and T-cell accumulation and long-term survival benefits. [23]
  • oncolytic herpes simplex virus (oHSV): Oncolytic herpes simplex virus (oHSV) therapies have been studied as intratumoral viral approaches that can reprogram the immunosuppressive glioblastoma microenvironment in preclinical and early clinical work. [23]

Radiotherapy

  • Hypofractionated radiotherapy plus temozolomide: When the harms of a 6-week radiotherapy plus temozolomide regimen may outweigh the benefits, hypofractionated radiotherapy plus temozolomide is stated as a reasonable option. [14]
    adjuvant duration 6 monthsstandard RT duration comparator 6 vs 6-week RT plus TMZ
    Source quotes
    • “Concurrent TMZ and RT should be offered to patients with newly diagnosed glioblastoma, IDH-wildtype, CNS WHO grade 4 followed by 6 months of adjuvant TMZ.”
    • “In situations in which the benefits of 6-week RT plus TMZ may not outweigh the harms, hypofractionated RT plus TMZ is reasonable.”
  • Radiotherapy · 2 findings
    • Adjuvant (after surgery)Radiotherapy is recommended using a single CTV definition based on postoperative contrast-enhanced T1 abnormalities and isotropic margins without the need to cone down, per the EORTC consensus cited by ESTRO-EANO. [19][6]
    • Radiotherapy is delivered as part of the standard post-resection regimen in combination with temozolomide as described in the Stupp protocol. [3]

Repurposed drugs

Show 1 lab & early-research entry
  • Suramin: Suramin inhibited telomerase activity in vitro in several tumor cell lines but was reported to increase telomerase activity in a C6 glioma brain tumor, an effect described as hormetic. [8]
    median overall survival with addition of temozolomide 14.6 vs 12.1 months vs postoperative radiotherapy alone
    Source quote
    • “This augmentation in median survival from 12.1 to 14.6 months was particularly beneficial to patients with methylation at the O6-methylguanine-DNA methyltransferase (MGMT) promoter in cancer DNA [3].”

Supplements & natural agents

Show 5 lab & early-research entries
  • Butylidenephthalide (BP): Butylidenephthalide (BP) inhibited proliferation and induced senescence in human GBM by downregulating hTERT expression and telomerase activity, reducing hTERT mRNA and telomerase activity within 48 h in vitro and repressing telomerase and inhibiting tumor proliferation in a mouse xenograft model. [8]
    median overall survival with addition of temozolomide 14.6 vs 12.1 months vs postoperative radiotherapy alone
    Source quote
    • “This augmentation in median survival from 12.1 to 14.6 months was particularly beneficial to patients with methylation at the O6-methylguanine-DNA methyltransferase (MGMT) promoter in cancer DNA [3].”
  • Costunolide: Costunolide (CS) has been reported to induce p53-mediated glioma cell death via reactive oxygen species (ROS) induction and to have telomerase-inhibitory effects in several in vitro studies. [8]
    median overall survival with addition of temozolomide 14.6 vs 12.1 months vs postoperative radiotherapy alone
    Source quote
    • “This augmentation in median survival from 12.1 to 14.6 months was particularly beneficial to patients with methylation at the O6-methylguanine-DNA methyltransferase (MGMT) promoter in cancer DNA [3].”
  • Epigallocatechin gallate (EGCG): Epigallocatechin gallate (EGCG) significantly reduced hTERT mRNA, telomerase activity, and cell growth rate in radioresistant glioma cells, inducing senescence and telomere-independent genotoxicity. [8]
    median overall survival with addition of temozolomide 14.6 vs 12.1 months vs postoperative radiotherapy alone
    Source quote
    • “This augmentation in median survival from 12.1 to 14.6 months was particularly beneficial to patients with methylation at the O6-methylguanine-DNA methyltransferase (MGMT) promoter in cancer DNA [3].”
  • Resveratrol: Resveratrol (RSV) significantly decreased hTERT mRNA expression in the GBM cell line U87MG, leading to reduced cell viability. [8]
    median overall survival with addition of temozolomide 14.6 vs 12.1 months vs postoperative radiotherapy alone
    Source quote
    • “This augmentation in median survival from 12.1 to 14.6 months was particularly beneficial to patients with methylation at the O6-methylguanine-DNA methyltransferase (MGMT) promoter in cancer DNA [3].”
  • Thymoquinone: Thymoquinone (TQ) induced cell death in GBM cell lines by inhibiting hTERT and reducing telomerase activity as assessed by TRAP. [8]
    median overall survival with addition of temozolomide 14.6 vs 12.1 months vs postoperative radiotherapy alone
    Source quote
    • “This augmentation in median survival from 12.1 to 14.6 months was particularly beneficial to patients with methylation at the O6-methylguanine-DNA methyltransferase (MGMT) promoter in cancer DNA [3].”

Procedures & devices

  • 5-aminolevulinic acid (5-ALA) fluorescence-guided surgery: 5-Aminolevulinic acid (5-ALA) fluorescence-guided surgery is described as a tool used to optimize surgical resection and was reported as cost-effective in a randomized trial cited in cost reviews. [6]
  • gross total resection (GTR): Gross total resection (GTR) has been used as a comparator and in pooled analyses was reported to have a statistically significant effect on median overall survival (SMD = 10.15 [2.74, 17.56]; p = 0.007). [1]
    SMD for median OS (GTR vs experimental) 10.15 (95% CI 2.74–17.56), p = 0.007 vs experimental groupHR for SMR vs GTR 0.9 (95% CI 0.84–0.97), p=0.005 vs GTRSMD for median PFS (SMR vs GTR) 10.21 (95% CI 4.3–16.12), p = 0.0007 vs GTR
    Source quotes
    • “As compared with the experimental group, GTR had a statistically significant effect on median OS (SMD = 10.15 [2.74, 17.56]; p = 0.007; I 2 = 80%).”
    • “Pooled analysis showed a statistically significant association of OS with SMR in GBM patients (HR = 0.90 [0.84, 0.97]; p = 0.005; I 2 = 96%)”
    • “Median PFS was significantly improved in the SMR group of GBM patients (SMD = 10.21 [4.30, 16.12]; p = 0.0007; I 2 = 0%).”
  • intraoperative radiotherapy: Intraoperative radiotherapy (IORT) for high-grade gliomas has been reported in observational series and meta-analysis to have an overall complication rate of 17% and survival rates at 12 and 24 months of 74% and 24%, respectively. [25]
    overall complication rate after IORT 17%IORT failure rate 77%12-month overall survival after IORT 74%24-month overall survival after IORT 24%
    Source quotes
    • “The overall complication rate after IORT was 17%, with significant heterogeneity observed.”
    • “The IORT failure rate was 77%, while the survival rates at 12 and 24months were 74% and 24%, respectively.”
    • “The IORT failure rate was 77%, while the survival rates at 12 and 24months were 74% and 24%, respectively.”
    • “The IORT failure rate was 77%, while the survival rates at 12 and 24months were 74% and 24%, respectively.”
  • Maximal safe surgical resection: Adjuvant (after surgery)Maximal safe surgical resection of the primary tumor is described as the initial intervention prior to adjuvant therapies in standard GBM care. [3]
  • Supratotal resection (SpTR): Supratotal resection (SpTR) was associated with significantly increased overall survival and progression-free survival when compared with other glioblastoma surgeries like GTR or SubTR. [18]
  • Surgical resection (extent of resection): First-line (advanced disease)EANS-EANO states that extent of resection may be associated with survival and impacts epilepsy, neurocognition, quality of life, neurological status, and planning of radiation and pharmacotherapy, and recommends resection of newly diagnosed glioblastomas (level A). [21]
  • Tumor Treating Fields (alternating electric field therapy): First-line (advanced disease)Alternating electric field therapy (tumor treating fields) is approved by the US FDA and ASCO-SNO states it should be considered for patients with newly diagnosed glioblastoma. [14]
    adjuvant duration 6 monthsstandard RT duration comparator 6 vs 6-week RT plus TMZ
    Source quotes
    • “Concurrent TMZ and RT should be offered to patients with newly diagnosed glioblastoma, IDH-wildtype, CNS WHO grade 4 followed by 6 months of adjuvant TMZ.”
    • “In situations in which the benefits of 6-week RT plus TMZ may not outweigh the harms, hypofractionated RT plus TMZ is reasonable.”
  • tumor treating fields (TTF): Sources list tumor treating fields in contemporary management and cost reviews as an adjunctive therapy used in GBM. [6]

Other

  • ?: Several targeted and other agents—including cediranib, regorafenib, enzastaurin, galunisertib, Depatux‑M, rindopepimut (EGFRvIII immunotherapy), onartuzumab (MET/VEGF), dasatinib, the viral gene therapy VB‑111, trebananib, nivolumab, and vorinostat—were evaluated in randomized or other trials for progressive glioblastoma. [7]
  • Best supportive care: For patients age 𐐐60 to 𐐐70 years with poor performance status or for whom toxicity or prognosis are concerns, ASCO-SNO states that best supportive care alone is a reasonable treatment option. [14]
    adjuvant duration 6 monthsstandard RT duration comparator 6 vs 6-week RT plus TMZ
    Source quotes
    • “Concurrent TMZ and RT should be offered to patients with newly diagnosed glioblastoma, IDH-wildtype, CNS WHO grade 4 followed by 6 months of adjuvant TMZ.”
    • “In situations in which the benefits of 6-week RT plus TMZ may not outweigh the harms, hypofractionated RT plus TMZ is reasonable.”
  • Graphene quantum dots (GQDs): Neoadjuvant (before surgery)Graphene quantum dots (GQDs) have been investigated in glioblastoma research for photothermal therapy, neoadjuvant (pretreatment) uses, biosensing, bioimaging, and drug delivery. [22]
  • supervised aerobic and resistance exercise: Adjuvant (after surgery)A supervised aerobic and resistance exercise intervention in people with primary brain tumours undergoing adjuvant chemoradiotherapy was reported not to cause seizures during clinical testing or moderate-intensity exercise. [26]
Show 1 lab & early-research entry
  • CRISPRi TERT silencing: A CRISPRi approach to transcriptionally silence TERT exon 1 and the TERT promoter was applied in GBM cell lines and patient-derived models, with authors reporting that TERT promoter‑mutant glioblastoma cells are dependent on telomerase and show features of telomere crisis when telomerase is lost. [8]
    median overall survival with addition of temozolomide 14.6 vs 12.1 months vs postoperative radiotherapy alone
    Source quote
    • “This augmentation in median survival from 12.1 to 14.6 months was particularly beneficial to patients with methylation at the O6-methylguanine-DNA methyltransferase (MGMT) promoter in cancer DNA [3].”
Prognosis11 points

Key figures

Prognostic factors
FactorEffectHR (95% CI)p
effect of histological grade in mGBM▲ worse1.633 (1.09–2.447)= 0.018
pooled hazard ratio for overall survival (mGBM vs hGBM) vs histological GBM (hGBM)▼ better0.824 (0.694–0.98)= 0.03
Source quotes
  • “In patients with mGBM, histological grade was a significant prognostic factor (pHR 1.633, [CI: 1.09-2.447], P = 0.018), as was age (P = 0.001) and surgical extent (P = 0.018).”
  • “Patients with mGBM had significantly longer OS times when compared to histological GBM (hGBM) (pooled hazard ratio (pHR) 0.824, [CI: 0.694-0.98], P = 0.03)).”
  • Sources report median overall survival with standard treatment variously as around 12–15 months, approximately 16 months, approximately 20 months, up to 15–26 months, and as less than 2 years. [2][22][9][7][3]5 sources
  • Sources report that over 50% of patients experience tumor recurrence within seven months of starting first-line treatment, and at least one source notes a nearly 100% recurrence rate and very poor long-term survival. [6][9]
  • Patients with molecular glioblastoma had significantly longer overall survival than patients with histological glioblastoma (pooled hazard ratio 0.824). [10]
  • In patients with mGBM, histological grade was reported as a significant prognostic factor (pHR 1.633); mGBM with grade II histology showed better overall survival rates compared to histological GBM. [10]
  • Age and surgical extent were reported as significant prognostic factors in patients with mGBM. [10]
  • A pooled analysis found that increasing age was significantly associated with decreased survival in GBM patients (HR = 1.03 [1.00, 1.05]; p = 0.02). [1]
  • Untreated glioblastoma median survival is reported as 3–4 months. [7]
  • Reported 5-year survival after glioblastoma diagnosis is less than 5%. [5]
  • The extent of resection may be associated with survival for gliomas. [21]
  • One review reported that median overall survival decreases to about 11 months in older patients. [22]
  • The inherent heterogeneity of GBM usually causes variations in prognosis, so overall survival time varies widely across individuals even when patients have the same tumor grade and receive similar treatments; accurate prediction of prognosis and survival for each patient is crucial to support personalized treatment decisions and to identify who may benefit from more or less aggressive therapy. [4]
Epidemiology8 points

Key figures

Survival & outcomes
OutcomeValue95% CI
5-year survival6.8%—
Source quotes
  • “Only 6.8% of patients survive beyond 5 years of initial diagnosis [1,2].”
  • Reported five-year survival for glioblastoma in systematic summaries ranges from about 4% to 17%. [26][8]
  • The occurrence/annual incidence of glioblastoma has been estimated at about 3 to 4 per 100,000 individuals; one report gave an annual incidence of 3.23 cases per 100,000 population in the United States. [22][7]
  • Glioblastoma (GBM) is the most frequent primary Central Nervous System (CNS) tumor in adults. [8]
  • In IDH wild-type lower-grade gliomas, the pooled mGBM rate was lower in Asian regions (43.7%) than in non-Asian regions (65.0%). [10]
  • In IDH-wildtype lower-grade gliomas, mGBM rates were significantly lower in fresh-frozen specimens than in formalin-fixed paraffin-embedded samples. [10]
  • GBM accounts for about half of all gliomas. [2]
  • Glioblastoma accounts for approximately 49% of malignant brain tumors. [9]
  • A pooled dataset in a socioeconomic-status meta-analysis included 230,601 patients. [13]
Biology & pathways5 points
  • Glioblastoma has an immunosuppressive tumor microenvironment characterized by low T-cell infiltration, myeloid dominance, dysfunctional antigen presentation, and strong local immunoregulatory signaling; tumor-associated macrophages and microglia make up the majority of immune cells in the glioblastoma niche and are described as promoting tumor growth through immunosuppression, angiogenesis, and extracellular matrix remodeling, and GBM has been described as a 'cold' tumour that creates an immunosuppressive microenvironment contributing to immune evasion and resistance to immunotherapy. [23][2]
  • Challenges in treating GBM include high infiltration, the blood–brain barrier's immunosuppressive role, and inter- and intra-tumour heterogeneity; GBM cellular heterogeneity and cellular plasticity include stem-like CD133+ populations that contribute to therapy evasion. [2][5]
  • Imaging and molecular integration analyses showed dysregulation of cell cycle, extracellular matrix organization, and immune infiltration or surveillance across GBM cases regardless of tumor location. [27]
  • A meta-analysis presented an integrated mechanistic model linking microRNAs associated with chemoresistance to downstream targets and pathways, and microRNAs upregulated in temozolomide resistance were predicted to target hundreds of mRNAs (400 predicted mRNA targets reported). [16]
  • Sources describe that telomerase, particularly hTERT promoter mutations present in up to 80% of GBM cases, sustains telomere length and cancer cell proliferation. [8]
Safety & interactions6 points

Key figures

Survival & outcomes
OutcomeValue95% CI
SMD for non-specified complications (SMR vs GTR)0.610.23–1.62
mortality rate reported in IORT series62%—
Source quotes
  • “An insignificant difference was noted in the rate of complications between the two groups of patients (SMD = 0.61 [0.23, 1.62]; p = 0.32; I 2 = 0%).”
  • “The mortality rate was 62%.”
  • In pooled analyses SMR was associated with a significantly lower mortality incidence compared with GTR (SMD = 0.20 [0.05, 0.84]; p = 0.03). [1]
  • In pooled reports of intraoperative radiotherapy (IORT) for high-grade gliomas, the overall reported mortality rate among included patients was 62%. [25]
  • Supervised moderate-intensity exercise in individuals with primary brain tumours undergoing adjuvant chemoradiotherapy was reported as not causing seizures in clinical testing. [26]
  • A meta-analysis reported an insignificant difference in perioperative complication rates between supramaximal resection (SMR) and gross-total resection (GTR) groups (SMD = 0.61 [0.23, 1.62]; p = 0.32). [1]
Show 2 lab & early-research findings
  • Wild-type herpes simplex virus is described as unsuitable for clinical use because of neurovirulence and the risk of severe encephalitis, and systemic interleukin-2 (IL-2) has prohibitive systemic toxicity when administered systemically; these safety concerns have prompted attenuation strategies and local delivery approaches for oncolytic HSV platforms in preclinical development. [23]
  • In preclinical studies, certain nitrogen- and boron-doped graphene quantum dots (GQDs) and other GQD formulations were assessed as biocompatible and showed no toxicity in vitro and in vivo at tested doses. [22]
What we don't know yet10 points
  • Machine learning and deep learning methods are being applied to predict GBM survival by combining pathology, histology, molecular, imaging, and clinical features, but the reporting, reproducibility, and methodological clarity of these approaches in GBM histopathology remain areas needing further work. [28][4]
  • Evidence for platelet-related prognostic factors in GBM is described as inconsistent and in need of further study. [12]
  • Evaluating whether compiled microRNA signatures improve progression-free and overall survival in GBM is proposed as a question for future study. [16]
  • Pre-clinical studies are developing artificial tumour microenvironments and anti-migratory (‘migrastatic’) drugs to control GBM migration and invasion. [2]
  • Authors of an IORT meta-analysis noted limitations including lack of control groups and small sample sizes and stated that prospective randomized controlled trials are needed. [25]
  • Socioeconomic factors (SES, race, insurance, area of residence) have been associated with differences in glioblastoma incidence and survival, and may confound observed outcomes. [13]
  • New therapies and specific tumor targets are urgently needed for GBM because current treatment options remain limited, and developing a successful telomerase inhibitor has been challenging despite telomerase being a compelling therapeutic target. [8]
  • The systematic review noted that risk of bias across studies was moderate. [10]
  • The meta-analysis suggested that alterations in post-translational modifications in MRI-classified GBM groups are noteworthy to explore for clinical applications. [27]
  • Interpretations of oHSV-induced microenvironmental reprogramming are framed as an emerging hypothesis derived largely from preclinical evidence rather than as a clinically validated therapeutic model. [23]
Staging & risk1 point
  • The Response Assessment in Neuro-Oncology (RANO) resect group defined categories for extent of resection based on contrast-enhancing (CE) and non-contrast-enhancing (nCE) residual tumor on postoperative MRI. [3]

Sources

Every statement above is drawn from these reviewed sources. This page reports what they describe. Sources last checked June 19, 2026.

  1. Meta-analysisEfficacy Assessment of Supramarginal Resection Versus Gross Total Resection in Glioblastoma: A Systematic Literature Review and Meta-Analysis · 2026
  2. Systematic reviewSystematic Review of Pre-Clinical Systems Using Artificial Microenvironments and Anti-Migratory Drugs to Control Migration of Glioblastoma Cells · 2025
  3. Systematic reviewPredicting glioblastoma progression using MR diffusion tensor imaging: A systematic review · 2025
  4. Systematic reviewSurvival prediction of glioblastoma patients using machine learning and deep learning: a systematic review · 2024
  5. Systematic reviewGlioblastoma research on zebrafish xenograft models: a systematic review · 2024
  6. Systematic reviewGlobal economic differences in modern glioblastoma care - a systematic review · 2026
  7. Meta-analysisTargeted agents in patients with progressive glioblastoma-A systematic meta-analysis of randomized clinical trials · 2024
  8. Systematic reviewAdvancements in Telomerase-Targeted Therapies for Glioblastoma: A Systematic Review · 2024
  9. Meta-analysisAnalysis of the correlation between inflammatory cytokines and glioblastoma: A Mendelian randomization study · 2025
  10. Meta-analysisIDH wild-type lower-grade gliomas with glioblastoma molecular features: a systematic review and meta-analysis · 2023
  11. GuidelineRadiation guidelines for gliomas · 2022
  12. Meta-analysisThe role of preoperative thrombocytic factors on survival in patients with glioblastoma: a meta-analysis and synopsis of the literature · 2026
  13. Meta-analysisSocioeconomic status as a determinant of survival in glioblastoma: a systematic review and meta-analysis · 2025
  14. GuidelineTherapy for Diffuse Astrocytic and Oligodendroglial Tumors in Adults: ASCO-SNO Guideline · 2022
  15. Meta-analysisRadiomics and deep learning models for predicting glioma p53 status: A diagnostic accuracy systematic review and meta-analysis of magnetic resonance imaging studies · 2026
  16. Meta-analysisInvestigating glioblastoma chemoresistance: a meta-analysis of microRNA signatures and gene networks · 2025
  17. GuidelineEANO guideline for the diagnosis and treatment of anaplastic gliomas and glioblastoma · 2014
  18. Meta-analysisSupratotal Resection: An Emerging Concept of Glioblastoma Multiforme Surgery-Systematic Review And Meta-Analysis · 2023
  19. GuidelineESTRO-EANO guideline on target delineation and radiotherapy details for glioblastoma · 2023
  20. GuidelineESTRO-ACROP guideline "target delineation of glioblastomas" · 2016
  21. GuidelineEANS-EANO guidelines on the extent of resection in gliomas · 2026
  22. Systematic reviewGraphene Quantum Dots for Glioblastoma Treatment and Detection-Systematic Review · 2025
  23. Systematic reviewReprogramming the Immunosuppressive Microenvironment in Glioblastoma Through Oncolytic Herpes Simplex Virus Therapy: A Systematic Review · 2026
  24. Meta-analysisDendritic cell vaccine for glioblastoma: an updated meta-analysis and trial sequential analysis · 2024
  25. Meta-analysisEfficacy and Safety of Intraoperative Radiotherapy for High-Grade Gliomas: A Systematic Review and Meta-Analysis · 2024
  26. Systematic reviewExercise Preferences, Barriers, Motivators, Facilitators, and Perceived Benefits in Adults With Brain Tumours-A Systematic Review · 2026
  27. Meta-analysisTakeaways from meta-analysis: indications of combinational treatments for glioblastoma · 2025
  28. Systematic reviewBrain tumour histopathology through the lens of deep learning: A systematic review · 2025

What supports this page

The kinds of sources behind this page, strongest at the top. Faint rungs show what is not here yet.

Guideline
8
Meta-analysis
85
Systematic review
65
Randomized trial
1
Clinical trial
14
Observational
2
Case report
28
Review
1173
Preclinical
0
Other
19

Living document — last change June 19, 2026: Cancer page updated. 4 recent updates logged.

Compounds compared by evidence

PubMed

How to read this: Ranked by the strength and volume of the evidence — NOT by how well a treatment works. A higher rank means a compound has been studied more, or in stronger study designs (e.g. randomized trials over lab studies), not that it produces better outcomes. The effect column shows the largest pooled figure reported, not a head-to-head comparison.

#CompoundEvidence strengthStudiesLargest pooled effect
1Temozolomide ChemotherapyLab only1—
2Bevacizumab Targeted therapyInsufficient evidence1—

Ranked across 2 compounds with published studies for this cancer. Updated 6/30/2026.

Medicines & supplements studied for Glioblastoma

PubMedFDAClinicalTrials.gov

Every drug, supplement, and other agent the published studies cover for Glioblastoma, ranked by how strong the evidence is — what studies report, not a recommendation. Tap any to see its full profile.

Medicines · 3

TemozolomideHuman trial / meta-analysisMixed results1 human1 lab

Includes human trial or meta-analysis evidence.

Largest credible effect: PFS hazard ratio 0.377 [0.217–0.653], p=0.0026 PMID 40466642 · median-survival values 12–31.6 across 4 studies

Most authoritative study: Efficacy and safety of adjuvant TTFields plus pembrolizumab and temozolomide in newly diagnosed glioblastoma: A phase 2 study

Findings conflict across studies · Effect sizes reported in only 1 of 6 studies.
ChemotherapyFDA approvedPhase 26 studiesFull profile →
PembrolizumabHuman trial / meta-analysisReported positive1 human

Includes human trial or meta-analysis evidence.

Largest credible effect: PFS hazard ratio 0.377 [0.217–0.653], p=0.0026 PMID 40466642 · median-survival values 12–31.6 across 4 studies

Most authoritative study: Efficacy and safety of adjuvant TTFields plus pembrolizumab and temozolomide in newly diagnosed glioblastoma: A phase 2 study

Based on a single study.
ImmunotherapyFDA off-labelPhase 21 studyFull profile →
BevacizumabInsufficient evidenceMixed results

No primary experimental studies yet.

Most authoritative study: Glioblastoma Treatment: State-of-the-Art and Future Perspectives

No human studies yet · No numeric effect sizes reported.
Targeted therapyFDA approved2 studiesFull profile →

What recent studies report in Glioblastoma

These are reviewed studies whose abstracts concern Glioblastoma. Each describes only what that study reported. This is not a claim by OncoForge that any compound helps or harms Glioblastoma. Most are early lab, animal, or small human studies, and findings often conflict.

54 studies7 human5 animal2 lab⚠ Conflicting evidenceMechanism (27)Trial (3)Formulation (1)Supportive care (1)

Tracking 54 published studies of Glioblastoma: 7 in humans, 5 in animals, 2 in the lab, 40 reviews/other.

Reported direction across studies: 24 positive, 12 mixed, 18 inconclusive.

Findings conflict — both supportive and negative/mixed results exist (see below). Human evidence is limited.

These counts summarize what the studies reported; they are not a measure of whether anything works for Glioblastoma.

Compounds with studies mentioning Glioblastoma

Temozolomide (6)Bevacizumab (2)Pembrolizumab (1)
Human · observationalMechanismInconclusiveLimited evidenceTier 3 · early human

Spatial patterns of glioblastoma

Cancer cell · Dec 2025 · spatial profiling of glioblastoma specimens

glioblastoma

The authors spatially profiled human glioblastoma specimens. They report uncovering cellular mechanisms that govern the extent of gene expression heterogeneity in malignant cells.

Key findings
  • The study performed spatial profiling of glioblastoma specimens.
  • The authors uncovered cellular mechanisms that govern the extent of gene expression heterogeneity in malignant cells.
Limitations: Abstract provides no sample size or details on patient cohorts.; Only descriptive spatial profiling of specimens is reported in the abstract; no therapeutic intervention or clinical trial data.; The abstract does not provide mechanistic details, validation experiments, or quantitative results..

AI summary of the abstract, human-reviewed · Jul 2026. Describes what this study reported, not medical advice. View on PubMed

ReviewMechanismReported positivePreclinical onlyTier 1 · lab

Glioblastoma hijacks cholinergic networks

Cancer cell · Nov 2025

glioblastoma

This Cancer Cell piece summarizes work by Yang et al. showing that glioblastoma co-opts cholinergic neural circuits. The authors describe mechanisms by which the tumor exploits cholinergic signaling to disrupt the hierarchical organization of brain networks and note that these findings change how we think about tumor–brain interactions and suggest potential therapeutic directions.

Key findings
  • Glioblastoma alters normal brain function by hijacking neural circuits.
  • Yang et al. elucidate mechanisms by which glioblastoma exploits cholinergic signaling pathways.
  • This hijacking disrupts the hierarchical organization of brain networks.
  • The analysis reframes tumor–brain interactions and is said to open new therapeutic avenues.
Limitations: Abstract is a short commentary/review and provides no experimental details or methods.; No species, model system, sample sizes, or quantitative results are reported in the abstract.; Unable to assess primary data, study design, or statistical strength from this abstract alone..

AI summary of the abstract, human-reviewed · Jul 2026. Describes what this study reported, not medical advice. View on PubMed

Animal studyMechanismReported positivePreclinical onlyTier 2 · animal

Now you serine, now you don't

Trends in pharmacological sciences · Nov 2025 · commentary/review of a study

glioblastomabrain neoplasms

This article discusses a study in glioblastoma showing that tumor cells took up more serine. It also reports that limiting serine uptake made chemoradiation work better in preclinical models. The abstract is mainly a commentary on emerging research rather than a full original trial report.

Studied with: chemoradiation.

Key findings
  • Tumor metabolism in glioblastoma patients showed increased import of serine.
  • Limiting serine uptake enhanced the effectiveness of chemoradiation in preclinical models of glioblastoma.
Limitations: This is not a full original study report; it is a commentary/review-style article.; The abstract does not provide methods, sample size, or quantitative results.; The sensitization finding is preclinical, so human clinical benefit is unproven..

Discusses a metabolic vulnerability in glioblastoma and preclinical chemoradiation sensitization.

AI summary of the abstract, human-reviewed · Jun 2026. Describes what this study reported, not medical advice. View on PubMed · Full text

Human · observationalMechanismMixed resultsLimited evidenceTier 3 · early human

Tumor treating fields alter local coagulation dynamics in glioblastoma patients

Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · Oct 2025

glioblastoma

The authors analyzed blood, tumor cells, and plasma-derived extracellular vesicles from glioblastoma patients and healthy donors to assess how Tumor Treating Fields (TTFields) affect coagulation-related biology. They report that short-term TTFields exposure prolonged blood coagulation and reduced clot rigidity by decreasing Factor II/FXIII activity and platelet count, while patient-derived GBM cells showed increased tissue factor (TF) abundance and changes in coagulation-related gene expression. Co-culture experiments indicated TTFields modulate pro- and anticoagulant factors and inflammatory pathways in the tumor microenvironment. The study does not report quantitative sample sizes or clinical thromboembolic outcomes.

Studied with: radiochemotherapy.

Key findings
  • Short-term TTFields exposure significantly prolongs blood coagulation in GBM patients and healthy donors by altering tissue factor (TF) expression and disrupting the extrinsic coagulation pathway.
  • TTFields reduced clot rigidity by decreasing Factor II/FXIII activity and platelet count, without impairing fibrinogen function.
  • Patient-derived GBM cells exposed to TTFields exhibited increased TF abundance.
  • RNA microarray of GBM cells after TTFields exposure showed upregulation of platelet adhesion marker ITGA2 and downregulation of THBS1.
  • TXNIP, described as a coagulation-modulating gene linked to immune regulation, was downregulated after TTFields exposure.
  • In an allogeneic co-culture model of patient-derived GBM cells and peripheral blood, TTFields modulated coagulation and immune responses, suggesting rebalancing of pro- and anticoagulant factors and alteration of inflammatory pathways.
Limitations: No sample size or detailed patient cohort characteristics are reported in the abstract.; Study reports short-term exposure effects; duration and long-term consequences are not defined.; Observational and ex vivo/in vitro analyses; causality in patients in vivo is not established.; No clinical outcome data on thromboembolic events or patient-level clinical endpoints are provided.; Findings include mixed pro- and anticoagulant signals (e.g., increased TF in tumor cells vs prolonged blood coagulation), complicating interpretation..

AI summary of the abstract, human-reviewed · Jul 2026. Describes what this study reported, not medical advice. View on PubMed · Full text

Human trialTrialReported positiveModerate evidenceTier 4 · clinicaln = 31

Efficacy and safety of adjuvant TTFields plus pembrolizumab and temozolomide in newly diagnosed glioblastoma: A phase 2 study

Med (New York, N.Y.) · Sep 2025 · Phase 2, single-arm with case-matched control comparison

This phase 2 clinical trial enrolled 31 patients with newly diagnosed glioblastoma after chemoradiation to test adding pembrolizumab to TTFields plus temozolomide. Among 26 patients treated per protocol, median progression-free survival was 12.0 vs. 5.8 months (HR 0.377; p = 0.0026) and median overall survival was 24.8 vs. 14.6 months (HR 0.522; p = 0.0477) compared to case-matched controls. Patients who had biopsy only showed larger PFS and OS benefits than those with maximal resection. Immune analyses suggested TTFields induced a T1IFN-driven clonal T cell expansion while pembrolizumab supported adaptive replacement and sustained T cell activation; severe treatment-related adverse events were reported as 7.5%.

Reported effects: median PFS 12 mo · PFS hazard ratio 0.377 [0.217–0.653], p=0.0026 · +7 more

Studied with: pembrolizumab, temozolomide.

Key findings
  • Among 26 patients treated per protocol, median PFS was 12.0 vs. 5.8 months in controls (HR 0.377, 95% CI 0.217-0.653; p = 0.0026).
  • Among 26 patients treated per protocol, median OS was 24.8 vs. 14.6 months in controls (HR 0.522, 95% CI 0.301-0.905; p = 0.0477).
  • Patients undergoing biopsy had longer PFS (27.2 vs. 9.6 months; HR 0.37, 95% CI 0.16-0.85; p = 0.014) and OS (31.6 vs. 18.8 months; HR 0.4, 95% CI 0.17-0.92; p = 0.023) compared to maximal resection.
  • Severe adverse events constituted 7.5% of treatment-related toxicities.
  • Immune correlates: TTFields promoted clonal T cell expansion via a T1IFN-driven trajectory, while pembrolizumab supported adaptive replacement of these clones, sustaining T cell activation and memory formation, especially in biopsy-only patients.
Limitations: Small sample size (31 enrolled; 26 treated per protocol).; Phase 2, non-randomized, single-arm design with case-matched controls rather than a randomized control group.; Potential selection or matching biases inherent to case-matched control comparisons.; Follow-up duration not specified in the abstract.; Funded by Novocure (industry support) which may present a conflict of interest..

AI summary of the abstract, human-reviewed · Jul 2026. Describes what this study reported, not medical advice. View on PubMed

ReviewReported positiveModerate evidenceTier 4 · clinical

Tumor treating fields for glioblastoma: opportunities and drawbacks

Expert review of medical devices · Sep 2025 · review

glioblastomabrain neoplasms

This review summarizes tumor treating fields (TTFields), an alternating electric-field therapy for glioblastoma that uses dielectrophoresis to disrupt mitosis in dividing cells. The authors state that clinical trials have shown TTFields added to standard adjuvant treatments significantly improved progression-free and overall survival. They also note unresolved questions about neuropsychological effects and management of postoperative motor deficits and call for further research.

Studied with: standard adjuvant treatments.

Key findings
  • TTFields therapy applies alternating electric fields and, via dielectrophoresis, selectively disrupts mitotic processes in replicating cells.
  • Clinical trials reported that TTFields significantly improved progression-free and overall survival rates when combined with standard adjuvant treatments.
  • Unanswered questions remain about the impact of TTFields on neuropsychological functioning and the management of postoperative motor deficits.
Limitations: This publication is a review rather than primary clinical trial data.; The abstract provides no numeric trial results or detailed quantitative outcomes.; The review notes unresolved clinical questions (neuropsychological effects, motor deficit management), indicating incomplete evidence.; Safety and long-term outcome details are not provided in the abstract..

AI summary of the abstract, human-reviewed · Jul 2026. Describes what this study reported, not medical advice. View on PubMed

ReviewReported positiveModerate evidenceTier 4 · clinical

Recent advances in Tumor Treating Fields (TTFields) therapy for glioblastoma

The oncologist · Feb 2025 · narrative review

glioblastomagrade 4 gliomapediatric central nervous system tumorsbrain metastaseslung cancerovarian cancerpancreatic cancergastric cancerhepatic cancer

This review summarizes Tumor Treating Fields (TTFields), a noninvasive device that delivers alternating electric fields to tumors. It reports mechanisms of action (mitotic disruption, DNA replication/DNA damage response effects, reduced motility, and immune enhancement), notes FDA approval for newly diagnosed and recurrent glioblastoma, and describes clinical data showing efficacy across patient groups, a tolerable safety profile, and correlations between higher device usage/dose and longer survival. The review also highlights promising pilot studies combining TTFields with immunotherapy and radiotherapy and ongoing studies in pediatric patients and other solid tumors.

Studied with: immunotherapy, radiotherapy.

Key findings
  • TTFields is a locoregional, noninvasive, portable device that delivers alternating electric fields to tumors through arrays placed on the skin.
  • Based on global pivotal randomized phase III clinical studies, TTFields therapy (Optune Gio) is FDA-approved for newly diagnosed and recurrent glioblastoma and CE-marked for grade 4 glioma.
  • Multimodal mechanisms include disruption of cancer cell mitosis, inhibition of DNA replication and damage response, interference with cell motility, and enhancement of systemic adaptive immunity.
  • Clinical data show efficacy in a broad range of patients with a tolerable safety profile, including high-risk subpopulations.
  • New analyses confirmed that overall and progression-free survival positively correlated with increased device usage and dose of TTFields at the tumor site.
  • Pilot/early phase clinical studies of TTFields with immunotherapy and with radiotherapy in newly diagnosed GBM have shown promise; new pivotal studies are planned.
  • Recent and ongoing studies are evaluating TTFields in pediatric care, other CNS tumors, brain metastases, and several advanced-stage solid tumors (lung, ovarian, pancreatic, gastric, hepatic).
Limitations: This article is a narrative review rather than original research; the abstract does not present new primary numeric results.; Abstract provides no numeric effect sizes, confidence intervals, p-values, or sample sizes for the studies discussed.; Claims about broader tumor types, pediatric use, and combinations are based on pilot/early-phase studies and ongoing research and thus remain preliminary.; Potential for selection or publication bias in the reviewed literature is not addressed in the abstract.; Funding sources and potential conflicts of interest are not reported in the abstract..

The review focuses on TTFields therapy's mechanisms, clinical efficacy/safety data in glioblastoma, and exploratory uses in other CNS and solid tumors.

AI summary of the abstract, human-reviewed · Jul 2026. Describes what this study reported, not medical advice. View on PubMed · Full text

Animal studyReported positivePreclinical onlyTier 2 · animal

Characterizing and targeting glioblastoma neuron-tumor networks with retrograde tracing

Cell · Jan 2025 · preclinical experimental study using retrograde tracing and genetic ablation in glioblastoma models

glioblastomabrain neoplasms

This study used rabies-virus-based retrograde tracing to map neurons connected to glioblastoma in experimental models. The authors found that glioblastoma formed widespread connections with neurons, and that cholinergic neurons promoted invasion. They also reported that radiotherapy increased neuron-tumor connectivity, while blocking neuronal activity together with radiotherapy had greater effects, and that genetic ablation of tumor-connected neurons halted glioblastoma progression in their models.

Studied with: radiotherapy.

Key findings
  • Glioblastoma integrated into neural circuits across the brain and showed widespread functional communication.
  • Cholinergic neurons were reported to drive glioblastoma invasion.
  • Radiotherapy increased neuron-tumor connectivity by increasing neuronal activity.
  • Simultaneous neuronal activity inhibition and radiotherapy showed increased therapeutic effects in the models.
  • Rabies-mediated genetic ablation of tumor-connected neurons halted glioblastoma progression in the study models.
Limitations: Preclinical animal/model-system study; no human clinical outcomes reported.; The abstract does not provide sample size, effect sizes, or statistical details.; Use of rabies-virus-based tracing and genetic ablation is experimental and not a standard clinical intervention.; Findings are based on glioblastoma models, so generalizability to patients is uncertain..

The study focuses on glioblastoma biology and experimental targeting of neuron-tumor networks, not on a repurposed drug or natural compound.

AI summary of the abstract, human-reviewed · Jun 2026. Describes what this study reported, not medical advice. View on PubMed

ReviewMechanismInconclusiveLimited evidenceTier 4 · clinical

Neuroinflammation in Glioblastoma: Progress and Perspectives

Brain sciences · Jul 2024

glioblastoma

This is a narrative review about neuroinflammation in glioblastoma. The authors summarize components of the tumor microenvironment, emphasize roles of resident and infiltrating inflammatory cells in glioblastoma pathogenesis, aggressiveness, and treatment resistance, and discuss anti-tumor microenvironment interventions as potential therapeutic targets.

Key findings
  • Glioblastoma has high morbidity and mortality despite multimodal treatment.
  • The tumor microenvironment is dynamic and heterogeneous and contains resident and infiltrating inflammatory cells.
  • Inflammatory cells within the tumor microenvironment regulate tumor aggressiveness and treatment resistance.
  • Targeting the tumor microenvironment, particularly neuroinflammation, is increasingly recognized as a potential therapeutic approach.
  • The review discusses interactions among tumor microenvironment components and potential anti-tumor microenvironment interventions.
Limitations: Review article with no new primary experimental or clinical data reported in the abstract.; Abstract does not specify whether this is a systematic review or a narrative review (possible selection bias).; No quantitative results, specific interventions, or clinical evidence are reported in the abstract..

AI summary of the abstract, human-reviewed · Jul 2026. Describes what this study reported, not medical advice. View on PubMed · Full text

Animal studyMechanismReported positivePreclinical onlyTier 2 · animal

Generation of glioblastoma in mice engrafted with human cytomegalovirus-infected astrocytes

Cancer gene therapy · Jul 2024

glioblastoma

Researchers isolated HCMV strains from glioblastoma tissues and used them to infect human astrocytes, transforming these cells into CMV-elicited glioblastoma cells (CEGBCs) that formed spheroids. When CEGBC-derived spheroids were orthotopically xenografted into mice they produced glioblastoma-like tumors that were nestin-positive in invasive regions, surrounded by GFAP-positive reactive astrocytes, showed EGFR and cMet gene amplification, and contained HCMV IE and UL69 genes and proteins.

Key findings
  • Three clinical HCMV strains isolated from glioblastoma tissues transformed human astrocytes into CMV-Elicited Glioblastoma Cells (CEGBCs).
  • Spheroids generated from CEGBCs produced glioblastoma-like tumors in orthotopically xenografted mice.
  • Resulting tumors were nestin-positive in invasive regions and were surrounded by GFAP-positive reactive astrocytes.
  • Tumors showed EGFR and cMet gene amplification and detection of HCMV IE and UL69 genes and proteins.
Limitations: Preclinical study using transformed human cells and mouse xenografts; no clinical/human outcome data provided.; Abstract provides no sample sizes, quantitative incidence, or statistical analysis.; Only three clinical HCMV strains are reported to have been isolated and tested (limited strain sampling).; No mention of control groups or negative controls in the abstract..

AI summary of the abstract, human-reviewed · Jul 2026. Describes what this study reported, not medical advice. View on PubMed · Full text

ReviewInconclusiveLimited evidenceTier 4 · clinical

Revolutionizing Glioblastoma Treatment: A Comprehensive Overview of Modern Therapeutic Approaches

International journal of molecular sciences · May 2024 · narrative review

glioblastoma

This narrative review summarizes modern treatment approaches for glioblastoma, beyond the standard surgery, radiotherapy and chemotherapy. It describes advanced local therapies (gamma knife, proton beam, tumor-treating fields), targeted agents (EGFR, VEGF, RTK and PI3K inhibitors) and immune-based strategies (CAR-T, CAR-NK, dendritic cell vaccines, checkpoint inhibitors). The authors note advantages and disadvantages of each approach and highlight challenges such as blood-brain barrier penetration, neurological/systemic side effects, and tumor immune-escape mechanisms.

Studied with: surgery, radiotherapy, chemotherapy.

Key findings
  • Standard multimodal treatment (surgery, radiotherapy, chemotherapy) yields limited survival in glioblastoma (background average survival cited as 12.1 to 14.6 months).
  • Advanced/local therapies discussed include gamma knife therapy, proton beam therapy, and tumor-treating fields.
  • Targeted therapies reviewed include EGFR and VEGF inhibitors, multiple RTK inhibitors, and PI3K pathway inhibitors.
  • Immunotherapies covered include CAR-T cells, CAR-NK cells, dendritic cell approaches, and immune checkpoint inhibitors.
  • Major challenges across methods include poor blood-brain barrier penetration, neurological and systemic side effects, and tumor escape mechanisms.
Limitations: Review article with no original patient-level or experimental data presented.; Narrative overview may not follow systematic review methodology (not stated in abstract).; Clinical efficacy and comparative effectiveness of the listed approaches are not established within this paper's abstract..

AI summary of the abstract, human-reviewed · Jul 2026. Describes what this study reported, not medical advice. View on PubMed · Full text

ReviewMixed resultsLimited evidenceTier 4 · clinical

Emerging Therapies for Glioblastoma

Cancers · Apr 2024 · review

Temozolomideglioblastoma

This narrative review summarizes emerging therapeutic approaches for glioblastoma, noting the disease's high heterogeneity and poor prognosis (approximately 12–18 months survival). It discusses limitations of conventional therapies (temozolomide, radiation, surgery) and reviews targeted pathways (PI3K, NF-kB, JAK-STAT, CK2, WNT, NOTCH, Hedgehog, TGF-beta) as well as oncolytic viruses and nanomaterials and their potential to improve blood–brain barrier penetration.

Key findings
  • Glioblastoma is highly heterogeneous and remains the most malignant primary brain tumor with an approximate survival of 12–18 months.
  • Conventional therapies (temozolomide, radiation, surgery) have limitations and there is currently no cure for glioblastoma.
  • The review discusses targeted therapeutic approaches to PI3K, NF-kB, JAK-STAT, CK2, WNT, NOTCH, Hedgehog, and TGF-beta pathways.
  • Oncolytic viruses and nanomaterials are described as highly novel applications, with progress in breaching the blood-brain barrier noted as a promising avenue for future therapies.
  • Despite many clinical trials, prognosis remains poor and further development of targeted and combination treatments is needed.
Limitations: Narrative review without original primary data reported in this paper (no new patient- or trial-level results).; Abstract provides only a high-level overview; specific clinical trial results, doses, sample sizes, and statistical outcomes are not provided.; Heterogeneous evidence base implied (preclinical and clinical) but not specified or graded in abstract.; No quantitative synthesis (e.g., meta-analysis) or methods described in abstract..

AI summary of the abstract, human-reviewed · Jul 2026. Describes what this study reported, not medical advice. View on PubMed · Full text

Browse all studies mentioning Glioblastoma →

Where the evidence is

What has been studied, and how strong it is, by topic. A dashed cell means no studies were found for that combination — a gap, not evidence of no effect. Open a row to see its studies.

CompoundHuman evidenceMechanismSafetyTrial
Temozolomide15—1
Pembrolizumab11—1
Bevacizumab—2——

Study mix

54 published studies by what they were done in. Lab and animal findings often do not carry over to people.

7 Human5 Animal2 Lab40 Review/other
Reported directionReported positive24Mixed results12Inconclusive18

Compounds with reported-positive results in Glioblastoma

Where at least one study reported a positive result, shown with the full picture, not just the wins. Positive results are more likely to be published, and most of these are early lab or animal studies that may not translate to people. This reports what studies found, not what works.

Human evidence

Temozolomide2 positive1 negative/mixed1 human1 lab
Limitations: Small sample size (31 enrolled; 26 treated per protocol).; Phase 2, non-randomized, single-arm design with case-matched controls rather than a randomized control group.; Potential selection or matching biases inherent to case-matched control comparisons.; Follow-up duration not specified in the abstract.; Funded by Novocure (industry support) which may present a conflict of interest.; In vitro cell-line study only; no animal or human outcomes..
Cited positive studies (2)
Pembrolizumab1 positive1 human
Limitations: Small sample size (31 enrolled; 26 treated per protocol).; Phase 2, non-randomized, single-arm design with case-matched controls rather than a randomized control group.; Potential selection or matching biases inherent to case-matched control comparisons.; Follow-up duration not specified in the abstract.; Funded by Novocure (industry support) which may present a conflict of interest..
Cited positive studies (1)

Evidence at a glance: compounds studied in Glioblastoma

A deterministic grade of what published studies report for each: strength of evidence, the reported direction, and the largest credible effect, strongest-evidence first. This summarizes findings; it is not a claim that anything works.

TemozolomideHuman trial / meta-analysisMixed results1 human1 lab

Includes human trial or meta-analysis evidence.

Largest credible effect: PFS hazard ratio 0.377 [0.217–0.653], p=0.0026 PMID 40466642 · median-survival values 12–31.6 across 4 studies

Most authoritative study: Efficacy and safety of adjuvant TTFields plus pembrolizumab and temozolomide in newly diagnosed glioblastoma: A phase 2 study

Findings conflict across studies · Effect sizes reported in only 1 of 6 studies.
PembrolizumabHuman trial / meta-analysisReported positive1 human

Includes human trial or meta-analysis evidence.

Largest credible effect: PFS hazard ratio 0.377 [0.217–0.653], p=0.0026 PMID 40466642 · median-survival values 12–31.6 across 4 studies

Most authoritative study: Efficacy and safety of adjuvant TTFields plus pembrolizumab and temozolomide in newly diagnosed glioblastoma: A phase 2 study

Based on a single study.
BevacizumabInsufficient evidenceMixed results

No primary experimental studies yet.

Most authoritative study: Glioblastoma Treatment: State-of-the-Art and Future Perspectives

No human studies yet · No numeric effect sizes reported.

Clinical trials in Glioblastoma

8 ongoing · 27 completed · tracked from ClinicalTrials.gov. Recruiting is not the same as proven, and completed is not the same as positive — read the results. Not a recommendation.

Completed
8 stopped (terminated / withdrawn / suspended)

Search all trials on ClinicalTrials.gov →

Getting care & support

Nonprofit / Gov

Practical, vetted help for Glioblastoma — advocacy, paying for treatment, second opinions, and caregivers.

If you’re struggling emotionally, you don’t have to wait.

Advocacy & community

No dedicated organization for this specific cancer is curated yet — these general organizations can help in the meantime.

Financial help

  • PAN Foundation ↗ — Copay assistance funds by diagnosis (funds open and close as money allows). · status changes often — check the fund’s site
  • HealthWell Foundation ↗ — Copay and premium assistance funds by disease. · status changes often — check the fund’s site
  • CancerCare — financial assistance ↗ — Limited grants plus free financial counseling. · status changes often — check the fund’s site
  • Family Reach ↗ — Help with everyday living costs (rent, transport, food) during treatment. · status changes often — check the fund’s site
  • NeedyMeds ↗ — Searchable directory of drug patient-assistance and discount programs. · status changes often — check the fund’s site
What you’ll typically need to apply
  • Your diagnosis and, if you have it, the specific drug/treatment name (from your care team).
  • Insurance details — your member ID card, or a note that you're uninsured (some funds require active insurance, some don't).
  • Proof of income and household size (recent pay stubs, a tax return, or a benefits letter) — most funds are income-based.
  • Your prescriber's contact information; some programs need the clinic to submit part of the application.
  • Apply early and re-check: funds open and close as money is available, so a closed fund may reopen.

General guidance — each program sets its own eligibility. Confirm requirements on the program’s site.

Help paying for the medicines on this page

Second opinions

Caregiver support

We list only non-profit and government resources — never product sellers — and take no affiliate fees. If a link is broken or a resource doesn't meet that bar, tell us.

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